ArticleProceedings of the National Academy of Sciences of the United States of America2006
FRA1 is a determinant for the difference in RAS-induced transformation between human and rat fibroblasts.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- ALKBH5 demethylation modification of SE-lncRNA ZMIZ1-AS1 promotes FGFR1-mediated proliferation and invasive metastasis in osteosarcoma.Cellular and molecular life sciences : CMLS · 2025Article
- FOSL1 is a key regulator of a super-enhancer driving TCOF1 expression in triple-negative breast cancer.Epigenetics & chromatin · 2024Article
- Overexpression of FRA1 (Cells · 2023Article
- FOSL1 promotes proneural-to-mesenchymal transition of glioblastoma stem cells via UBC9/CYLD/NF-κB axis.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Review
- Combined computational and intracellular peptide library screening: towards a potent and selective Fra1 inhibitor.RSC chemical biology · 2021Article
- An integrative approach unveils FOSL1 as an oncogene vulnerability in KRAS-driven lung and pancreatic cancer.Nature communications · 2017Article
- All for one and FOSL1 for all: FOSL1 at the crossroads of lung and pancreatic cancer driven by mutant KRAS.Molecular & cellular oncology · 2017Article
- The Fra-1-miR-134-SDS22 feedback loop amplifies ERK/JNK signaling and reduces chemosensitivity in ovarian cancer cells.Cell death & disease · 2016Article
- FRA1 promotes squamous cell carcinoma growth and metastasis through distinct AKT and c-Jun dependent mechanisms.Oncotarget · 2016Article
- Different Roles of Negative and Positive Components of the Circadian Clock in Oncogene-induced Neoplastic Transformation.The Journal of biological chemistry · 2016Article
- FRA-1 as a driver of tumour heterogeneity: a nexus between oncogenes and embryonic signalling pathways in cancer.Oncogene · 2015Review
- Fate and plasticity of the epidermis in response to congenital activation of BRAF.The Journal of investigative dermatology · 2015Article
- Protein kinase C α is a central signaling node and therapeutic target for breast cancer stem cells.Cancer cell · 2013Article
- A 19S proteasomal subunit cooperates with an ERK MAPK-regulated degron to regulate accumulation of Fra-1 in tumour cells.Oncogene · 2012Article
- Fra-1 controls motility of bladder cancer cells via transcriptional upregulation of the receptor tyrosine kinase AXL.Oncogene · 2012Article
- ERK2 but not ERK1 induces epithelial-to-mesenchymal transformation via DEF motif-dependent signaling events.Molecular cell · 2010Article
- O6-methylguanine-DNA methyltransferase is downregulated in transformed astrocyte cells: implications for anti-glioma therapies.Molecular cancer · 2007Article
- Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human diploid fibroblasts (HDF) immortalized by hTERT and simian virus 40 (SV40) early region (ER) exhibit a limited degree of transformation upon the expression of activated H-RAS (H-RAS V12) compared with rat embryonic fibroblasts (REF) immortalized by SV40 ER. Here, we identified FRA1 as a determinant for this difference in RAS-induced transformation. FRA1 was not induced by H-RAS V12 in the immortalized HDF, in contrast to its marked accumulation in the immortalized REF. Ectopic expression of FRA1 significantly enhanced anchorage-independent growth of various HDF expressing hTERT, SV40 ER, and H-RAS V12. More importantly, FRA1 could induce anchorage-independent growth as well as nude mice tumor formation of the immortalized HDF in the absence of H-RAS V12. The results of an in vitro kinase assay clearly showed that the RAS-induced extracellular signal-regulated kinase (ERK) activation, which is responsible for FRA1 induction, was markedly attenuated in the HDF compared with that in the REF, despite no obvious differences in the phosphorylation status of ERK between the species. Our results strongly suggest that HDF negatively regulate the mitogen-activated protein kinase kinase (MEK)/ERK pathway more efficiently than REF, and consequently express less malignant phenotypes in response to H-RAS V12.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.